title: Reduced plasma fibrin clot permeability and susceptibility to lysis in patients with inflammatory bowel disease: a novel prothrombotic mechanism.
abstract: BACKGROUND
  Inflammatory bowel disease (IBD) is associated with an increased risk of thromboembolism. Its mechanism is still unclear. Altered fibrin clot properties have been reported in patients with thromboembolism and those with chronic inflammatory states. We investigated whether fibrin characteristics are abnormal in IBD.
  
  
  METHODS
  Ex vivo plasma fibrin clot permeability (Ks), compaction, turbidity, and efficiency of fibrinolysis were assessed in 85 consecutive patients with IBD, including 47 with ulcerative colitis (UC) and 38 with Crohn's disease (CD), all with no history of thromboembolism. Forty-eight patients matched for age and sex served as controls.
  
  
  RESULTS
  Compared with controls, patients with UC and CD had 29.5% and 35.7% lower Ks associated with 13.8% and 23.1% lower compaction, respectively (all P < 0.001). Patients with UC and CD had higher maximum clot absorbance (+8.9%, P = 0.008, and +15.2%, P < 0.0001, respectively), higher maximum D-dimer released from clots (D-D(max), +27.0%, P = 0.01, and +28.7%, P < 0.0001, respectively), and prolonged clot lysis time (+19.0%, P < 0.0001, and +25.5%, P < 0.0001, respectively). Lag phase was similar in both group of patients. D-D(max) was the only parameter that differed between patients in the UC and CD groups, being higher in CD (P = 0.04). The multiple linear regression model showed that in patients with UC, but not with CD, Ks, compaction, lysis time, and D-D(max) were all independently associated with disease activity. In patients with CD, Ks and lysis time were independently predicted by fibrinogen and C-reactive protein.
  
  
  CONCLUSIONS
  Both UC and CD are characterized by formation of dense fibrin networks relatively resistant to lysis. Prothrombotic clot phenotype might represent a novel mechanism increasing thrombotic risk in IBD.
authors.affiliation: *Department of Gastroenterology, Hepatology and Infectious Diseases, Jagiellonian University Medical College, Kraków, Poland; †Department of Bioinformatics and Telemedicine, Jagiellonian University Medical College, Kraków, Poland; and ‡Institute of Cardiology, Jagiellonian University Medical College, and John Paul II Hospital, Kraków, Poland.
authors.forename: Danuta
authors.initials: D
authors.lastname: Owczarek
authors.forename: Dorota
authors.initials: D
authors.lastname: Cibor
authors.forename: Kinga
authors.initials: K
authors.lastname: Sałapa
authors.forename: Mikołaj K
authors.initials: MK
authors.lastname: Głowacki
authors.forename: Tomasz
authors.initials: T
authors.lastname: Mach
authors.forename: Anetta
authors.initials: A
authors.lastname: Undas
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D003093:Colitis, Ulcerative / Q000150:complications* / Q000473:pathology; D003424:Crohn Disease / Q000150:complications* / Q000473:pathology; D005260:Female; D005337:Fibrin / Q000737:chemistry* / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D005342:Fibrinolysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D010539:Permeability; D011379:Prognosis; D012307:Risk Factors; D015996:Survival Rate; D013927:Thrombosis / Q000097:blood / Q000209:etiology*; D055815:Young Adult
chemical_list: D005337:Fibrin; D005340:Fibrinogen; D002097:C-Reactive Protein